Human mucous membranes, generally colonized by commensal bacteria, are the habitat that is most exposed to the aggression of pathogenic microorganisms and viruses. In physiological situations, mucosal secretions, constituted by several proteins and peptides of natural immunity, ensure protection against microbial and viral attack. Inflammatory response is a fundamental defense mechanism against infections which is implemented by the host, but in some conditions it can become so intense as to be harmful. In such cases, the immunotolerance of the host with respect to commensal microorganisms becomes an adaptive immune response against pathogens, which creates an inflammation which is termed “destructive” because it is always accompanied by significant damage to the cells of the host. Therefore, the balance between physiological inflammation and destructive inflammation, together with the regulatory mechanisms that limit inflammatory response and restore, when necessary, homeostasis of the inflammation (physiological inflammation), are essential, because they ensure inhibition of destructive phenomena which might, for example, combine with damage caused by infectious disorders already in progress, and the mucous membranes themselves, damaged and lacking the non-antibody factors of natural immunity, might become more susceptible to the onset of any infection. The onset of a pathological and destructive inflammation can be caused by the persistence of a stimulus that the body recognizes as foreign and tends to eliminate unsuccessfully. Typical cases are, for example, destructive inflammations following more or less pathological pregnancies, and especially following viral infections, mycoses or infections caused by bacteria (both Gram-positive and Gram-negative) which are localized intracellularly or which, once they have adhered to the cells of the body, synthesize, and cover themselves, with a more or less thick layer of polysaccharides, which together with the microorganisms constitutes the so-called biofilm, which is known to be impermeable to ordinary bactericidal and bacteriostatic agents.
One common and important incidental disorder of destructive inflammation is constituted by more or less severe states of hypoferremia and/or anemia. During inflammation there is in fact a gradual transfer of free iron from circulation to the tissues, increasing considerably the physiological concentration of free iron at the mucus membrane level (approximately 10−18 M). This fact has several harmful consequences for the body, including (i) an overproduction, at tissue level, of reactive oxygen species, above all superoxides (by means of the iron-induced Fenton reaction), and (ii) an increase in the production of proinflammatory cytokines. Moreover, it has been demonstrated that an increase in the iron that is available or free at the level of the mucous membranes facilitates microbial and viral proliferation and dissemination, since many pathogens exhibit both growth and virulence induced by iron. Finally, the presence of infections of the mucous membranes of the oral cavity (for example parodontopathies), of the intestine (enteritides) or of the vaginal epithelium in progress, in turn leads to bleeding and to a further withdrawal of iron from circulation; these factors increase the overload of iron in the tissues (to the point of creating states of chronic anemia caused by infections and consequent inflammations), in a sort of positive feedback. All of the above explains why the onset of a destructive phlogosis at the level of the mucous membranes is often associated with pathological conditions of hypoferremia and/or anemia and/or infections affecting said mucous membranes, to the point in which the roles of cause and consequence among the various disorders are hard to distinguish.
Currently, states of chronic inflammation possibly associated with hypoferremia, anemia and acute or chronic infections are treated by administering substances that are specific for each symptom, such as antibiotics, antivirals, antiinflammatories or iron-based therapies, thus requiring the combination of drug cocktails if two or more of these complications are present simultaneously. However, there are no drugs capable of having an appreciable therapeutic effect on more than one component simultaneously.
The aim of the present invention is, therefore, to provide for the use of a substance for preparing a medicament for preventing and/or treating destructive inflammation affecting mucous membranes, optionally associated with states of hypoferremia and/or anemia and/or acute or chronic infections.
Within the scope of this aim, an object is to provide a composition for treating and preventing the therapeutic indications mentioned above which allows to achieve a particularly effective and potent effect.